Transcript twist project

Left Ventricular Twist Mechanics in Heart Failure:
Evolving Role in the Assessment of Cardiac Dyssynchrony
M Bertini, PP Sengupta, G Nucifora, V Delgado, ACT Ng,
N Ajmone Marsan, M Shanks, RJ van Bommel, MJ Schalij, J Narula, JJ Bax
JACC Cardiovascular Imaging 2009
Disclosures
• Jeroen Bax received grants from Medtronic,
Boston Scientific, Biotronik, St. Jude Medical, BMS
medical imaging, Edwards Lifesciences & GE
Healthcare
• Martin Schalij received grants from Biotronik,
Medtronic & Boston Scientific
Introduction
 The opposite rotation of LV apex
and base leads to a LV systolic
wringing motion during systole
referred to as twist.
 LV twist contributes significantly to LV
systolic function
 LV twist is an important aspect of
cardiac mechanics that may be
useful to characterize HF
patients and effects of CRT on HF
Objects of the Review:
1. Overview of physiology of LV rotational mechanics;
2. Discussion on different LV twist patterns in systolic HF;
3. The evolving role of LV twist as a marker of LV dyssynchrony
for understanding response to CRT.
Normal LV Twist Mechanics
LV Twist is affected by:
1. Preload (directly related to LV end-diastolic volume)
2. Afterload (inversely related to LV end-systolic volume)
3. Contractility (directly related to positive inotropic interventions)
4. Increase gradually from infancy to adulthood
LV Twist in the Dyssynchronous, Failing
Ventricle
Ischemic vs. Non-ischemic Failing Ventricle:
LV twist is more reduced in HF as compared to acute myocardial infarction
Different mechanisms underlying the reduction in LV twist:
1. In HF patients, LV twist impairment results from a long-standing process,
with a rearrangement of LV myofibers and loss of the specific LV architecture.
2. In acute myocardial infarction, the LV twist reduction may result from
an acute impairment in rotation of the LV region that is involved in the infarction.
LV Twist in the Dyssynchronous, Failing
Ventricle
Relation LV Twist-Dyssynchrony:
Deleterious effects of asynchronous ventricular activation on LV performance
and the relation between the LV activation pattern and LV twist
RV pacing may determine
a dyssynchronous mechanical activation
and a deterioration of LV twist
LV Twist in CRT
Zhang et al. (Heart 2008): 39 HF pts
• LV twist reduced in HF as compared to
normal
• Improvement of LVEF 3 months after CRT
• No improvement of LV twist 3 months
after CRT
Sade et al. (Am J Cardiol 2008): 33 HF pts
• LV twist reduced in HF as compared to
normal
• Improvement of LVEF immediately after CRT
• Improvement of LV twist immediately after
CRT
Bertini et al. (J Am Coll Cardiol 2009): 80 HF pts
• LV twist reduced in HF as compared to
normal
• Improvement of LVEF immediately after and
6 months after CRT
• Improvement of LV twist immediately after
and 6 months after CRT
LV Twist in CRT
Responders vs. Non-responders
LV twist progressively
improved in responders
Gradual deterioration
of LV twist in non-responders
LV Twist in CRT
LV Twist and LV Lead Position
Postero-lateral LV leads
positioned in mid-ventricular
and apical as compared to
basal regions had a larger
increase in systolic function
with a significant increase in
LV twist
Conclusions



LV twist mechanics is a promising tool for characterizing the
pathophysiology of HF.
In advanced systolic HF, the rotational parameters are severely
deteriorated and may be improved by restoring electro-mechanical
activation through CRT.
LV lead position is important for modifying the extent of LV twist after
CRT; in particular pacing sites which provide the greatest
improvement of LV twist likely determine the largest reversal of LV
remodeling after CRT